Consider Vitamin D in Alzheimer's Prevention and Management

This transcript has been edited for clarity.

I'm Richard Isaacson, director of the Alzheimer's Prevention Clinic at Weill Cornell Medicine and NewYork-Presbyterian.

Over the years, evolving evidence has helped our understanding of whether vitamin D has any potential neuroprotective or therapeutic effect when it comes to Alzheimer's disease. During that time, we've learned more and more about the relationship between vitamin D and other neurologic conditions, such as multiple sclerosis, and its potential protective effects and mechanisms. But from a practical clinical perspective, what is the real story with vitamin D and Alzheimer's prevention and treatment?

When you look at epidemiologic data, it does appear that vitamin D potentially has a protective effect when it comes to Alzheimer's disease. Does that mean that vitamin D should be utilized when trying to reduce a person's risk for Alzheimer's? Well, it depends. If a person's vitamin D level is 25 (nmol/L), 20, or lower, then maybe it makes some practical sense that we should, at a minimum, try to target a vitamin D level above 30. However, an important 2014 study in the journal Neurology^[1] investigating the optimal target level for vitamin D suggests that aiming toward 50 nmol/L may have a better therapeutic effect when it comes to prevention and risk reduction for dementia.

What about when it comes to treatment? Should patients who are already diagnosed with Alzheimer's disease be on vitamin D supplementation? Again, this may not be one-size-fits-all. It could be that we need to consider levels, or that different people with different genes need different therapies.

A recent study^[2] from China suggests that there actually may be a role for vitamin D supplementation in this area. Investigators randomized 210 people (105 in each arm) with Alzheimer's disease to 800 IU/day of vitamin D or placebo for 12 months. They looked not only at the potential beneficial effects of vitamin D supplementation on cognitive function, but also at its impact on Alzheimer's disease biomarkers like amyloid beta. Although the study was small and conducted at only one center, it was nonetheless positive in showing that vitamin D supplementation not only improved various measures of cognitive function in people already diagnosed with the earliest phases of Alzheimer's, but it also had a positive impact on Alzheimer's disease biomarkers. The question is, did the vitamin D actually have a disease-modifying or potentially direct beneficial effect on disease pathophysiology?

Although more studies are definitely needed, vitamin D is a relatively safe intervention. We need to realize that 800 IU is not a super-high dose. However, various doses and forms of vitamin D have been investigated in other studies, and we really don't have all the answers just yet.

When it comes to risk reduction for Alzheimer's disease, I also think there may be a genetic contribution, as shown in the emerging fields of pharmacogenomics and nutrigenomics. A study published several years ago in the European Journal of Clinical Nutrition^[3] helped us fine-tune our potential suggestions by showing that people with two APOE ɛ4 alleles may have had a preferential benefit from vitamin D supplementation.

In conclusion, I would say that vitamin D is generally safe and that it is potentially effective as well. When it comes to risk reduction, as well as for treatment of patients with early Alzheimer's disease, vitamin D may very well be one of our new therapeutic paradigms.

Richard Isaacson is an associate professor in the Department of Neurology at Weill Cornell Medicine in New York City. In 2013 he founded the first Alzheimer's disease prevention clinic in the United States and is a leading advocate for the idea that cognitive decline can be prevented or slowed through lifestyle interventions.

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